PubMed · 14596918
Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells.
Abstract
Akt is activated by growth factors to regulate various aspects of vascular smooth muscle cell function. Platelet-derived growth factor (PDGF) and insulin-like growth factor-1 activated Akt in vascular smooth muscle cells with a rapid reduction of total Akt protein that lasted for several hours. The downregulation of Akt required phosphatidylinositol 3-kinase activity, but not intrinsic Akt activity. The downregulation of Akt was abrogated by MG-132, a proteasome inhibitor, but not by inhibitors of calpain or cathepsins. Akt was found in ubiquitin immune complex after PDGF treatment. Proteasome-dependent degradation of Akt may provide a counter-regulatory mechanism against overactivation of Akt.
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Mayumi Adachi, Koichi Ricardo Katsumura, Kozo Fujii, Sei Kobayashi, Hiroki Aoki, Masunori Matsuzaki. 2003-11-06. Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells.. https://doi.org/10.1016/s0014-5793(03)01109-8
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